Brown-adipose-tissue lipogenesis in starvation: effects of insulin and (_)hydroxycitrate

Sugden, Mary C.; Watts, David; Marshall, C.E.; McCormack, James G.

doi:10.1007/bf01115114

Cited by 28 publications

(28 citation statements)

References 22 publications

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“…Indeed, in brown fat, rates of lipogenesis after 6 h starvation were not significantly different from those observed after 48 h starvation (Table 2), when lipogenic rates may be sustained by increased use of non-carbohydrate precursors, which may include ketone bodies (Agius & Williamson, 1981) or acetate (Steiner & Cahill, 1966;Sugden et al, 1982).…”

Section: Methodsmentioning

confidence: 82%

Pyruvate dehydrogenase activities and rates of lipogenesis during the fed-to-starved transition in liver and brown adipose tissue of the rat

Holness

Sugden

1990

Biochemical Journal

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The percentages of pyruvate dehydrogenase complex (PDH) in the active form (PDHa) in two lipogenic tissues (liver and brown adipose tissue) in the fed state were 12.00% and 13.40% respectively. After acute (0.5 h) insulin treatment, PDHa activities had increased by 77 % in liver and by 234 % in brown fat. Significant decreases in PDHa activities were observed in both tissues by 5 h after the removal of food. The patterns of decline in PDHa activities in the two lipogenic tissues were similar in that the major decreases in activities were observed within the first 7 h of starvation. The significant decreases in PDHa activities observed after starvation for 6 h were accompanied by decreased rates of lipogenesis. Hepatic and brown-fat PDHa activities after acute (30 min) exposure to exogenous insulin were less in 6 h-starved than in fed rats, but the absolute increases in PDHa activities over the 30 min exposure period were similar in fed and 6 h-starved rats. Increases in PDHa activities were paralleled by increases in lipid synthesis in both tissues. Re-activation of PDH in response to insulin treatment or chow re-feeding after 48 h starvation occurred more rapidly in brown adipose tissue than in liver. The results are discussed in relation to the importance of the activity of the PDH complex as a determinant of the total rate of lipogenesis during the fed-to-starved transition and after insulin challenge or re-feeding.

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Section: Methodsmentioning

confidence: 82%

Pyruvate dehydrogenase activities and rates of lipogenesis during the fed-to-starved transition in liver and brown adipose tissue of the rat

Holness

Sugden

1990

Biochemical Journal

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“…This can be taken to indicate greater stimulation of acetyl-CoA carboxylase than of fatty acid synthase in response to re-feeding. Lipogenic substrates after chow re-feeding Hepatic lipogenesis in starved rats is insensitive to inhibition of ATP citrate lyase by (-)-hydroxycitrate [11,28,29]. The increases in lipogenic rates observed between 2 h and 4 h after chow administration to 48 hstarved rats (Fig.…”

Section: Blood Metabolite Concentrations After Chow Re-feedingmentioning

confidence: 92%

“…In some experiments, (-)-hydroxycitrate (0.85,usmol/100 g body wt. in 0.15 MNaCl, pH 7.4) was given at the time of administration of 3H20 (see [11] for details).…”

Section: Introductionmentioning

confidence: 99%

The disposition of carbohydrate between glycogenesis, lipogenesis and oxidation in liver during the starved-to-fed transition

Holness

Maclennan

Palmer

et al. 1988

Biochemical Journal

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A comparison was made between the time courses of restoration of pyruvate dehydrogenase activities, fructose 2,6-bisphosphate concentrations and lipogenic rates, together with net hepatic glucose flux and glycogen synthesis/deposition in livers of 48 h-starved rats provided with laboratory chow ad libitum for up to 24 h. Increased glycogenesis, lipogenesis and net glucose uptake were observed after 1 h of re-feeding, preceding re-activation of pyruvate dehydrogenase, which occurred after 3-4 h. Increased concentrations of fructose 2,6-bisphosphate were only observed after 5-6 h. The implication of the temporal relationship between these parameters is discussed.

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“…Due to the fact that Nat8l silencing does not contrarily influence lipogenesis, we wondered whether another acetyl-CoAproducing pathway might be up-regulated to compensate for the decreased NAA-derived acetyl-CoA. Indeed, we found ATP-citrate lyase, the cytosolic enzyme converting citrate to acetyl-CoA and thereby linking cellular glucose catabolism and lipogenesis (33), significantly increased in both Nat8l-silenced iBACs and BAT of Nat8l-KO mice, whereas it was unchanged in Nat8l-overexpressing iBACs when compared with the respective controls (Fig. 7H).…”

Section: Nat8l Silencing In Ibacs and Knock-out Of Nat8l In Mice Leadmentioning

confidence: 99%

NAT8L (N-Acetyltransferase 8-Like) Accelerates Lipid Turnover and Increases Energy Expenditure in Brown Adipocytes

Pessentheiner

Pelzmann

Walenta

et al. 2013

Journal of Biological Chemistry

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Background: NAT8L (N-acetyltransferase 8-like) synthesizes N-acetylaspartate and is required for myelination in the brain. Its function in other tissues was undefined. Results: Nat8l is highly expressed in adipose tissues and impacts adipogenic marker gene expression, lipid turnover, and energy metabolism in brown adipocytes. Conclusion: Nat8l expression influences cellular bioenergetics in adipocytes. Significance: These findings establish a novel pathway in brown adipocyte metabolism.

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Brown-adipose-tissue lipogenesis in starvation: effects of insulin and (_)hydroxycitrate

Cited by 28 publications

References 22 publications

Pyruvate dehydrogenase activities and rates of lipogenesis during the fed-to-starved transition in liver and brown adipose tissue of the rat

Pyruvate dehydrogenase activities and rates of lipogenesis during the fed-to-starved transition in liver and brown adipose tissue of the rat

The disposition of carbohydrate between glycogenesis, lipogenesis and oxidation in liver during the starved-to-fed transition

NAT8L (N-Acetyltransferase 8-Like) Accelerates Lipid Turnover and Increases Energy Expenditure in Brown Adipocytes

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